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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

ABSTRACT: GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

PROVIDER: PRJNA826839 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18753136.fastq.gz	Fastqsanger.gz
	SRR18753137.fastq.gz	Fastqsanger.gz
	SRR18753138.fastq.gz	Fastqsanger.gz
	SRR18753139.fastq.gz	Fastqsanger.gz
	SRR18753140.fastq.gz	Fastqsanger.gz

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

Project description:GPR174 is abundantly expressed in B and T lymphocytes and has a role in restraining T cell responses, but the function of GPR174 in B cells is less clear. Here we report that upon in vitro culture B cells undergo a spontaneous GPR174-dependent activation process that is associated with marked changes in gene expression, including upregulation of Cd86, Nr4a1, Ccr7 and phosphodiesterases. B cells lacking Gas show a block in induction of the GPR174-dependent program. Spontaneous upregulation of CD86 in cultured B cells is dependent on protein kinase A. Both GPR174- and Gas-deficient B cells show enhanced survival in culture. In vivo, GPR174 contributes to NUR77 expression in follicular B cells and is needed for establishing a marginal zone compartment of normal size. Treatment of mice with lysophosphatidylserine (lysoPS), a GPR174 ligand, is sufficient to promote CD86 upregulation by follicular B cells. These findings demonstrate that GPR174 can signal via Gas to modulate B cell gene expression and show this can occur in vivo in response to lysoPS. Additionally, the findings illuminate a pathway that might be targeted to improve systems for the in vitro study of B cell responses.

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-16 | GSE200800 | GEO

GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

Project description:Regulatory T cells (Tregs) are critically involved in neovascularization, an important compensatory mechanism in peripheral artery disease (PAD). The contribution of G protein coupled receptor 174 (GPR174), which is a regulator of Treg function and development, in neovascularization remains elusive. Here, we reveal that genetic deletion of GPR174 in Tregs potentiated blood flow recovery in mice after hindlimb ischemia (HLI). GPR174 deficiency upregulates amphiregulin (AREG) expression in Tregs, thereby enhancing endothelial cell functions and reducing pro-inflammatory macrophage polarization and endothelial cell apoptosis. Mechanically, GPR174 regulates AREG expression by inhibiting the nuclear accumulation of early growth response protein 1 (EGR1) via Gαs/cAMP/PKA signal pathway activation. Collectively, these findings demonstrate that GPR174 negatively regulates angiogenesis and vascular remodeling in response to ischemic injury and that GPR174 may be a potential molecular target for therapeutic interventions of ischemic vascular diseases.

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GPR174 signals via G<i>α</i>s to control a CD86-containing gene expression program in B cells.

Project description:GPR174 is abundantly expressed in B and T lymphocytes and has a role in restraining T cell responses, but the function of GPR174 in B cells is less clear. Here we report that upon in vitro culture B cells undergo a spontaneous GPR174-dependent activation process that is associated with marked changes in gene expression, including up-regulation of Cd86, Nr4a1, Ccr7, and phosphodiesterases. B cells lacking Gαs show a block in induction of the GPR174-dependent program. Spontaneous up-regulation of CD86 in cultured B cells is dependent on protein kinase A. Both GPR174- and Gαs-deficient B cells show enhanced survival in culture. In vivo, GPR174 contributes to NUR77 expression in follicular B cells and is needed for establishing a marginal zone compartment of normal size. Treatment of mice with lysophosphatidylserine (lysoPS), a GPR174 ligand, is sufficient to promote CD86 up-regulation by follicular B cells. These findings demonstrate that GPR174 can signal via Gαs to modulate B cell gene expression and show this can occur in vivo in response to lysoPS. Additionally, the findings illuminate a pathway that might be targeted to improve systems for the in vitro study of B cell responses.

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